scholarly journals Acute kidney injury and disseminated intravascular coagulation due to mercuric chloride poisoning

2016 ◽  
Vol 26 (3) ◽  
pp. 206 ◽  
Author(s):  
J Dhanapriya ◽  
N Gopalakrishnan ◽  
V Arun ◽  
T Dineshkumar ◽  
R Sakthirajan ◽  
...  
2016 ◽  
Vol 36 (2) ◽  
pp. 213-217 ◽  
Author(s):  
Rajniti Prasad ◽  
Om P. Mishra

Background Acute kidney injury (AKI) in P. falciparum malaria infection is an important morbidity in children. The purpose of the present study was done to observe the renal involvement, associated morbidities and outcome. Methods Out of 156 patients with severe P. falciparum malaria, diagnosed on the basis of compatible clinical presentations and positive malarial parasites in the peripheral blood smear and/or histidine rich protein 2 antigen, 31 had AKI at presentation and were analyzed. Results Of 31 (19.9%) patients with AKI, 4 were classified at risk, 11 injury, and 16 failure stage, as per pRIFLE criteria (pediatric version of RIFLE [R = risk, I = injury, F = failure, L = loss E = end-stage kidney disease]). Mean age of children with AKI was 7.7 ± 3.2 years. A significantly higher proportion of patients with AKI had hypoglycemia (41.9%), pulmonary edema (32.2%), and disseminated intravascular coagulation (DIC) (29.0%) compared to those without AKI (18.4%, 4.8%, and 3.2%, respectively). Twelve patients (38.7%) required peritoneal dialysis (PD), 8 (25.8%) died, and all were in failure stage. The non-survivors had significantly higher blood urea ( p = 0.005) and serum creatinine levels ( p = 0.042), lower glomerular filtration rate ( p < 0.001), longer duration of illness ( p = 0.003), and oliguria/anuria ( p = 0.001) than survivors at admission. On logistic regression analysis, the disseminated intravascular coagulation (DIC), jaundice and parasite density (≥ 3+) were found to be significant factors contributing to mortality in children with AKI. Conclusions Acute kidney injury in falciparum malaria is one of the severe systemic complications. Duration of illness and presence of comorbidities adversely affected the outcome.


2021 ◽  
Vol 6 (2) ◽  
pp. 01-05
Author(s):  
Gurwant Kaur

Introduction Purpura fulminans (PF) is a life-threatening syndrome consisting of Disseminated Intravascular Coagulation (DIC), thrombotic occlusion of small- and medium-sized blood vessels with skin necrosis. Although there are few studies in the literature, only a minority of them discuss renal manifestations. Case Report We present a case of a 57-year-old Caucasian female with acute kidney injury (AKI) in the setting of multiorgan failure (MOF), DIC and PF. She presented with fever, exudative drainage from her port site, and skin changes concerning for bacteremia. Empiric antibiotics were started after blood, urine, and wound cultures were obtained. None of the cultures grew any organisms. Fever resolved after port removal. She exhibited thrombocytopenia, leukopenia, and neutropenia. Urinalysis showed hyaline casts and a fractional excretion of urea (FeUrea) ≤35% indicating a pre-renal state. Her hospital course was complicated by atrial fibrillation, acute hypoxic respiratory failure requiring mechanical ventilation, and hypovolemic shock requiring pressor support. Further, complicated by multiorgan failure including non-oliguric AKI and heart failure with reduced ejection fraction (HFrEF) of ≤65%. Acute skin findings included dusky, purple macules and patches involving all digits of both hands as well as gangrenous changes on the face and toes. It prompted further investigation by Hematology and Dermatology. Skin biopsy showed early leukocytoclastic vasculitis changes. Her laboratory markers were suggestive of DIC and Purpura Fulminans.


2020 ◽  
Author(s):  
Alina Bianca Giurgiu ◽  
Ina Maria Kacso ◽  
Daniela Ionescu ◽  
Radu Badea

We report the case of a sepsis-induced acute kidney injury accompanied by disseminated intravascular coagulation and thrombotic microangiopathy, responsible for subsequent renal microvascular thrombosis. Contrast-enhanced ultrasound was used to assess the thrombotic cortical kidney ischemia and its evolution over time.


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